Alterations in arterial CO2 rather than pH affect the kinetics of neurovascular coupling in humans
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Alterations in arterial CO2 rather than pH affect the kinetics of neurovascular coupling in humans. / Caldwell, Hannah Grace; Howe, Connor A; Hoiland, Ryan L; Carr, Jay M J R; Chalifoux, Carter J; Brown, Courtney V; Patrician, Alexander; Tremblay, Joshua C; Panerai, Ronney B; Robinson, Thompson G; Minhas, Jatinder S; Ainslie, Philip N.
I: Journal of Physiology, Bind 599, Nr. 15, 2021, s. 3663-3676.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Alterations in arterial CO2 rather than pH affect the kinetics of neurovascular coupling in humans
AU - Caldwell, Hannah Grace
AU - Howe, Connor A
AU - Hoiland, Ryan L
AU - Carr, Jay M J R
AU - Chalifoux, Carter J
AU - Brown, Courtney V
AU - Patrician, Alexander
AU - Tremblay, Joshua C
AU - Panerai, Ronney B
AU - Robinson, Thompson G
AU - Minhas, Jatinder S
AU - Ainslie, Philip N
N1 - (Ekstern)
PY - 2021
Y1 - 2021
N2 - Elevations in cerebral metabolism necessitate appropriate coordinated and localized increases in cerebral blood flow (i.e. neurovascular coupling; NVC). Recent pre-clinical work indicates that arterial PCO2 (PaCO2) mediates NVC independently of arterial/extracellular pH; this has yet to be experimentally tested in humans. The goal of this study was to investigate the hypotheses that: (1) the NVC response would be unaffected by acute experimentally elevated arterial pH; rather, PaCO2 would regulate any changes in NVC; and (2) stepwise respiratory alkalosis and acidosis would each progressively reduce the NVC response. Ten healthy males completed a standardized visual stimulus-evoked NVC test during matched stepwise iso-oxic alterations in PaCO2 (hypocapnia: −5, −10 mmHg; hypercapnia: +5, +10 mmHg) prior to and following intravenous NaHCO3 (8.4%, 50 mEq/50 ml) that elevated arterial pH (7.406 ± 0.019 vs. 7.457 ± 0.029; P < 0.001) and [HCO3–] (26.2 ± 1.5 vs. 29.3 ± 0.9 mEq/l; P < 0.001). Although the NVC response was collectively attenuated by 27–38% with −10 mmHg PaCO2 (stage post hoc: all P < 0.05), this response was unaltered following NaHCO3 (all P > 0.05) irrespective of the higher pH (P = 0.002) at each matched stage of PaCO2 (P = 0.417). The absolute peak change was reduced by −19 ± 41% with +10 mmHg PaCO2 irrespective of acutely elevated arterial pH/[HCO3–] (stage post hoc: P = 0.022). The NVC kinetics (i.e. time to peak) were markedly slower with hypercapnia versus hypocapnia (24 ± 5 vs. 7 ± 5 s, respectively; stage effect: P < 0.001). Overall, these findings indicate that temporal patterns in NVC are acutely regulated by PaCO2 rather than arterial pH per se in the setting of acute metabolic alkalosis in humans.
AB - Elevations in cerebral metabolism necessitate appropriate coordinated and localized increases in cerebral blood flow (i.e. neurovascular coupling; NVC). Recent pre-clinical work indicates that arterial PCO2 (PaCO2) mediates NVC independently of arterial/extracellular pH; this has yet to be experimentally tested in humans. The goal of this study was to investigate the hypotheses that: (1) the NVC response would be unaffected by acute experimentally elevated arterial pH; rather, PaCO2 would regulate any changes in NVC; and (2) stepwise respiratory alkalosis and acidosis would each progressively reduce the NVC response. Ten healthy males completed a standardized visual stimulus-evoked NVC test during matched stepwise iso-oxic alterations in PaCO2 (hypocapnia: −5, −10 mmHg; hypercapnia: +5, +10 mmHg) prior to and following intravenous NaHCO3 (8.4%, 50 mEq/50 ml) that elevated arterial pH (7.406 ± 0.019 vs. 7.457 ± 0.029; P < 0.001) and [HCO3–] (26.2 ± 1.5 vs. 29.3 ± 0.9 mEq/l; P < 0.001). Although the NVC response was collectively attenuated by 27–38% with −10 mmHg PaCO2 (stage post hoc: all P < 0.05), this response was unaltered following NaHCO3 (all P > 0.05) irrespective of the higher pH (P = 0.002) at each matched stage of PaCO2 (P = 0.417). The absolute peak change was reduced by −19 ± 41% with +10 mmHg PaCO2 irrespective of acutely elevated arterial pH/[HCO3–] (stage post hoc: P = 0.022). The NVC kinetics (i.e. time to peak) were markedly slower with hypercapnia versus hypocapnia (24 ± 5 vs. 7 ± 5 s, respectively; stage effect: P < 0.001). Overall, these findings indicate that temporal patterns in NVC are acutely regulated by PaCO2 rather than arterial pH per se in the setting of acute metabolic alkalosis in humans.
U2 - 10.1113/JP281615
DO - 10.1113/JP281615
M3 - Journal article
C2 - 34107079
VL - 599
SP - 3663
EP - 3676
JO - The Journal of Physiology
JF - The Journal of Physiology
SN - 0022-3751
IS - 15
ER -
ID: 273078392